Abstract
The aim of this study was to assess if women with a low first trimester maternal pregnancy-associated plasma protein-A (PAPP-A) level are at increased risk of emergency cesarean (EmCS) for intrapartum fetal compromise (IFC) and/or adverse neonatal outcomes. This was a retrospective cohort study performed at Mater Mother’s Hospital, Brisbane, Australia, between 2016 and 2018. All women with a singleton, euploid, non-anomalous fetus with a documented PAPP-A level measured between 10 +0 and 13 +6 weeks gestation during the study period were included. Data were extracted from the institution’s perinatal database and dichotomized according to PAPP-A level (≤0.4 Multiples of Medium (MoM) vs. >0.4 MoM). The primary outcomes were EmCS-IFC and a composite of severe adverse neonatal outcomes (SCNO). Nine thousand sixty-one pregnancies were included, 3.3% with a PAPP-A ≤ 0.4 MoM. Low maternal PAPP-A was not associated with an increased risk of EmCS-IFC (adjusted odds ratio (aOR) 0.77, 95% confidence interval (CI) 0.24–2.46, p = 0.66) or SCNO (aOR 0.65, 95% CI 0.39–1.07, p = 0.09). Low PAPP-A was associated with increased odds of pre-eclampsia, preterm birth and birthweight < 10th centile. In conclusion, low maternal PAPP-A level is not associated with an increased risk of EmCS IFC or adverse neonatal outcomes despite greater odds of low-birthweight infants and preterm birth.
Highlights
Fetal hypoxia in labor occurs when there is a mismatch between utero-placental perfusion and fetal oxygen and metabolic requirements in between uterine contractions [1,2]
Given the association between maternal plasma protein-A (PAPP-A) levels and placental function, we investigated the correlation between first trimester PAPP-A levels and the risk of emergency cesarean section (EmCS) for intrapartum fetal compromise (IFC) (“fetal distress”) and adverse neonatal outcomes
Low PAPP-A levels did not increase the odds of EmCS IFC (1.0% vs. 1.3%; aOR 0.77, 95% CI 0.24–2.46, p = 0.66)
Summary
Fetal hypoxia in labor occurs when there is a mismatch between utero-placental perfusion and fetal oxygen and metabolic requirements in between uterine contractions [1,2]. Whilst most fetuses can tolerate the reduction in placental perfusion during labor, some cannot and are at risk of hypoxic injury [3]. Perinatal hypoxia is a major contributor to a myriad of adverse outcomes, including stillbirth, neonatal death, hypoxic ischemic encephalopathy and severe neonatal morbidity. Pregnancies that are complicated by pre-existing placental dysfunction, regardless of the size of the fetus, are at increased risk of perinatal complications [3,6,7,8]. Identification of pre-existing placental dysfunction is the focus of considerable research effort
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